ABSTRACT
Parkinson’s disease (PD) is a progressive neuropathological condition affecting 2% of people over 65 years and is visually characterized by muscle rigidity, resting tremor, and bradykinesia [1]. Following the initial description of these symptoms by James Parkinson, observations made by Brissaud, Tretiakoff, and Lewy led to the conclusion that the primary neuropathological lesion of PD is the degeneration of neuromelanin-containing dopamine neurons of the substantia nigra pars compacta (SNpc), characteristically associated with eosinophilic inclusions or Lewy bodies [2]. Although the neuropathology and symptomatology are well dened [3], there is still no clear evidence to explain the etiology for dopaminergic neuron loss in PD. The etiology of PD is hypothesized to result from a genetic predisposition, exposure to an environmental agent, or a combination of these factors [4-7]. There is evidence to suggest that the cell death of SNpc dopamine neurons in PD can occur through either an uncontrolled mechanism known commonly as necrosis or through a genetically dened series of programmed steps commonly known as apoptosis [8,9]. The induction of these processes may be initiated by ubiquitin-proteasomal and autophagy-lysosomal system dysfunction, oxidative stress and free radical formation, mitochondrial dysfunction, inŸammation, excitotoxicity, calcium dysregulation, and loss of neurotrophic factors [10,11].
